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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

The classic features of obesity hypoventilation syndrome (OHS) are obesity and daytime hypercapnia.[1] The differences between OHS and obstructive sleep apnoea (OSA) are that the former has:[2]

Longer and more continuous episodes of hypoventilation overnight (there may or may not be upper airway obstruction).

Daytime hypercapnia.

Pathophysiology

Controversy surrounds the pathophysiology. Only a small proportion of morbidly obese patients suffer from the condition, so factors other than obesity must be at work. Some authors believe that the basic problem relates to the way the ventilatory drive reacts to hypoxia and hypercapnia.[3] Others consider that fat distribution, hormones and upper airway size are involved.

Upper airway obstruction is certainly known to play a prominent role. It may be associated with rapid eye movement (REM) atonia, increased fat distribution around the neck and upward displacement of the diaphragm by abdominal fat.[4] Experiments with mouse models suggest that deficiency of or resistance to leptin (a substance which reduces the surface tension of lung tissue) may be involved, leading to alterations in central respiratory drive and reduced ventilatory responsiveness, permitting development of carbon dioxide retention. Changes in neuromodulators resulting from the effects of hypoxia may further exacerbate the problem by depressing arousal from sleep in the face of abnormal breathing.[1]

Differentiation has been made between people suffering from sleep apnoea and obesity hypoventilation syndrome (OHS) in which hypoventilation is also evident whilst they are awake.[5] Most patients with the syndrome also have sleep apnoea but some patients do not, suggesting that it is the obesity per se which is causing chronic hypoventilation.[6]

Patients may also have concomitant features of asthma or chronic obstructive pulmonary disease (COPD).

Epidemiology

There are no figures available for incidence or prevalence, mainly because the condition has been poorly defined in the past and often confused with obstructive sleep apnoea (OSA). It has been estimated that approximately 10-20% of patients with OSA have obesity hypoventilation syndrome (OHS).[3] Risk factors mirror that for obesity and the condition is more common in females. Tonsillar hypertrophy is an aggravating factor in children. The peak ages of presentation are 5-7 years and adolescence,[4] although increased awareness of the condition means that more and more cases are being diagnosed in adults.[2]

A drug history should be taken to exclude alcohol excess, sedating antihistamines and central nervous system depressants, all of which can aggravate the condition.

The typical patient will be clinically obese, with marked fat deposition around the chin and abdomen. Thoracic kyphosis is often a feature. Leg oedema may be present.

The head, ears, nose and throat should be examined to exclude facial dysmorphologies or ENT abnormalities that may cause upper airway obstruction, such as macroglossia, micrognathia, retrognathia or high-arched palate. The tonsils should be examined to exclude hypertrophy and the nasal passages to exclude polyps, cysts or swollen nasal turbinates.

Examination of the chest may reveal signs of cor pulmonale (loud second heart sound, displaced cardiac impulse). Acquired pes excavatum may result from overuse of the respiratory muscles overcoming extrathoracic obstruction.

Diagnosis

Obesity hypoventilation syndrome (OHS) cannot be diagnosed on history and examination alone but requires the demonstration of daytime hypercapnia.[6]

Nocturnal oximetry should be carried out to determine whether sleep apnoea is also present (about one fifth of sleep apnoeic patients will have obesity hypoventilation syndrome (OHS). Formal polysomnography may be required in borderline cases.

CXR - may show chest wall deformities, or signs of cardiomegaly or congestive failure.

A return to normal bodyweight is the mainstay of treatment. Unfortunately, although they may lose weight initially, many patients are non-compliant with dietary restriction in the long term. They are furthermore restricted from increasing their physical activity due to pulmonary symptoms. Bariatric surgery may be required in severe cases.

Continuous positive airways pressure (CPAP) is more helpful in obstructive sleep apnoea (OSA), where as patients with obesity hypoventilation syndrome (OHS) usually need assisted ventilation which may need to be supplemented by oxygen.

The inability of these patients to increase their ventilatory capacity should be borne in mind during their management (eg when they are subjected to hospital procedures which may lead to hypercapnia).[8]

Treat any concomitant OSA, asthma or COPD as appropriate.

Complications

Chronic hypoventilation may be associated with congestive heart failure, cor pulmonale and angina. Future research is likely to focus on the links between the syndrome and cardiovascular morbidity.[9] Early epidemiological data suggest a link with coronary artery disease and stroke.[10]

Disclaimer: This article is for information only and should not be used for
the diagnosis or treatment of medical conditions. EMIS has used all reasonable care
in compiling the information but make no warranty as to its accuracy. Consult a
doctor or other health care professional for diagnosis and treatment of medical
conditions. For details see our conditions.